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Effect of Menaquinone-7 (MK-7) Supplementation on Anthropometric Measurements, Glycemic Indices, and Lipid Profiles: A Systematic Review and Meta-Analysis of Randomized Controlled Trials 补充甲基萘醌-7 (MK-7)对人体测量、血糖指数和脂质谱的影响:随机对照试验的系统评价和荟萃分析
IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-03-01 DOI: 10.1016/j.prostaglandins.2025.106970
Omid Nikpayam , Ali Jafari , Amirhossein Faghfouri , Mohammadjavad Pasand , Pardis Noura , Marziyeh Najafi , Golbon Sohrab

Background

Menaquinone-7 (MK-7) is a type of vitamin K that has a longer half-life and stays in the body for a more extended period compared to other types of vitamin K. Recently, the effects of this vitamin on body weight, glycemic control, and lipid profiles have garnered much attention. Aim of the review: This systematic review and meta-analysis were performed to evaluate the effects of MK-7 on anthropometric measurements, glycemic indices, and lipid profiles.

Methods

A systematic search via appropriate keywords was conducted in electronic databases including PubMed, Scopus, Web of Science, and Google Scholar up to October 2023 to obtain relevant original articles. The quality of studies was evaluated using the Cochrane Collaboration tool. Six original articles met our criteria and were included in the analysis.

Results

Statistical analysis showed that MK-7 had a desirable effect on inulin (SMD= −0.56; 95 % CI: −0.77, −0.36; P = 0.000, I2 = 84 %, P = 0.000), HbA1c (SMD=-0.32; 95 % CI: −0.55, −0.09; P = 0.007, I2 = 86.8 %, P = 0.000), and homeostatic Model Assessment for Insulin Resistance (HOMA-IR) (SMD= −0.56; 95 % CI: −0.76, −0.35; P = 0.000, I2 = 84.3 %, P = 0.000). Additionally, subgroup analysis revealed negligible effects of MK-7 on total cholesterol (TC), insulin, HbA1c, and HOMA-IR in both genders of patients who received ≤ 90 mg MK-7 for less than 12 weeks. However, MK-7 didn’t have any meaningful effect on other factors.

Conclusion

Based on the findings of the present systematic review and meta-analysis, MK-7 may have beneficial effects on glycemic control and TC, although further highly qualified original research is needed for a consistent conclusion.
背景:与其他类型的维生素K相比,甲基萘醌-7 (MK-7)是一种半衰期更长、在体内停留时间更长的维生素K。最近,这种维生素对体重、血糖控制和脂质谱的影响引起了人们的广泛关注。综述的目的:本系统综述和荟萃分析旨在评估MK-7对人体测量、血糖指数和脂质谱的影响。方法:在PubMed、Scopus、Web of Science、谷歌Scholar等截止到2023年10月的电子数据库中,通过合适的关键词进行系统检索,获取相关原创文章。使用Cochrane协作工具评估研究的质量。六篇符合我们标准的原创文章被纳入分析。结果:经统计分析,MK-7对菊粉有较好的效果(SMD= -0.56;95% ci: -0.77, -0.36;P=0.000, I2= 84%, P=0.000), HbA1c (SMD=-0.32;95% ci: -0.55, -0.09;P=0.007, I2= 86.8%, P=0.000),以及胰岛素抵抗稳态模型评估(HOMA-IR) (SMD= -0.56;95% ci: -0.76, -0.35;P=0.000, i2 = 84.3%, P=0.000)。此外,亚组分析显示,在接受≤90mg MK-7治疗不足12周的男女患者中,MK-7对总胆固醇(TC)、胰岛素、HbA1c和HOMA-IR的影响可以忽略不计。然而,MK-7对其他因素没有显著影响。结论:基于本系统综述和荟萃分析的结果,MK-7可能对血糖控制和TC有有益作用,尽管需要进一步的高质量的原始研究来得出一致的结论。
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引用次数: 0
An editorial farewell 编辑告别。
IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-03-01 DOI: 10.1016/j.prostaglandins.2025.106950
Michal Laniado Schwartzman
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引用次数: 0
The interplay of LDLR, PCSK9, and lncRNA- LASER genes expression in coronary artery disease: Implications for therapeutic interventions 冠状动脉疾病中 LDLR、PCSK9 和 lncRNA- LASER 基因表达的相互作用:对治疗干预的影响。
IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-03-01 DOI: 10.1016/j.prostaglandins.2025.106969
Tayebe Ghiasvand , Jamshid Karimi , Iraj Khodadadi , Amirhossein Yazdi , Salman Khazaei , Zahra Abedi kichi , Seyed Kianoosh Hosseini

Background and purpose

Coronary artery disease (CAD) is defined as stenosis of coronary arteries due to atherosclerosis. The etiology of atherosclerosis can be attributed to a disruption in lipid metabolism, specifically cholesterol and low-density lipoprotein cholesterol (LDL-C). PCSK9 is an enzyme that controls the metabolism of LDL-C by degrading the low-density lipoprotein receptor (LDLR), which in turn affects the metabolism of LDL-C. A newly discovered Long Non-coding RNA named LASER, which affects the homeostasis of cholesterol, has been identified through the evaluation of bioinformatics. The objective of this study was to assess the levels of gene expression related to cholesterol balance, specifically LDLR, PCSK9, and LASER, in peripheral blood mononuclear cells (PBMCs) of Iranian CAD patients in comparison to controls.

Experimental approach

This case-control study included 49 CAD patients, with 81.63 % receiving statins, compared to 40 control subjects, of whom 40 % received statins. The qRT-PCR was used to analyze the expression levels of LDLR, PCSK9, and LASER in PBMCs. Additionally, the ELISA method was employed to determine the blood concentration of PCSK9.

Findings / results

CAD patients demonstrated a significant reduction in PBMC gene expression levels of LDLR (P < 0.01) and a significant rise in gene expression of PCSK9 and LASER, as well as blood concentration of PCSK9 (P < 0.05) compared to controls. The gene expression of PCSK9 showed a strong positive relationship with LDLR expression in patients (P = 0.0003). Furthermore, a strong correlation was seen between PCSK9 and LASER, as well as LASER and LDLR expression (P < 0.0001) in two groups.

Conclusion and implications

PCSK9 and LASER are potential therapeutic targets for atherosclerosis-related disorders, including CAD. Given that patients receiving statins were twice that of the control subjects, and the effect of statins on the LDLR, PCSK9 and LASER, further research is required to delineate the distinct effects of coronary artery disease conditions and statin usage on the expression of the aforementioned genes.
背景与目的:冠状动脉疾病(CAD)是指由动脉粥样硬化引起的冠状动脉狭窄。动脉粥样硬化的病因可归因于脂质代谢的破坏,特别是胆固醇和低密度脂蛋白胆固醇(LDL-C)。PCSK9是一种通过降解低密度脂蛋白受体(LDLR)来控制LDL-C代谢的酶,LDLR反过来影响LDL-C的代谢。通过生物信息学评价,新发现了一种影响胆固醇稳态的长链非编码RNA LASER。本研究的目的是评估伊朗CAD患者外周血单个核细胞(PBMCs)中与胆固醇平衡相关的基因表达水平,特别是LDLR、PCSK9和LASER。实验方法:本病例对照研究纳入49例CAD患者,其中81.63%接受他汀类药物治疗,对照组40例,其中40%接受他汀类药物治疗。采用qRT-PCR分析pbmc中LDLR、PCSK9和LASER的表达水平。采用ELISA法测定PCSK9血药浓度。结果:与对照组相比,患者LDLR中PBMC基因表达水平显著降低(P < 0.01), PCSK9、LASER基因表达及PCSK9血药浓度显著升高(P < 0.05)。PCSK9基因表达与患者LDLR表达呈显著正相关(P = 0.0003)。在两组中,PCSK9与LASER、LASER与LDLR的表达有较强的相关性(P < 0.0001)。结论和意义:PCSK9和LASER是动脉粥样硬化相关疾病(包括CAD)的潜在治疗靶点。考虑到接受他汀类药物治疗的患者是对照组的两倍,以及他汀类药物对LDLR、PCSK9和LASER的影响,需要进一步的研究来描述冠状动脉疾病状况和他汀类药物使用对上述基因表达的明显影响。
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引用次数: 0
Involvement of COX inhibitor and arachidonic acid in manipulating obesity and obesity-induced bone resorption markers in obese mice COX抑制剂和花生四烯酸参与控制肥胖小鼠的肥胖和肥胖诱导的骨吸收标志物
IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-03-01 DOI: 10.1016/j.prostaglandins.2025.106971
Rahima Begum, Sourav Roy, Md. Abdur Rahman Ripon, Mohammad Tohidul Amin, Mohammad Salim Hossain
Obesity and bone-loss have remained a focus of research. Obesity stimulates adipose tissue expansion and adipocyte hypertrophy, resulting in chronic low-grade inflammation in the adipocytes. This enlarged adipocyte secretes a variety of pro-inflammatory chemicals. Because of their endocrine signaling, these substances indirectly promote osteoclast activity and bone-loss. However, the role of COX-2 signaling in obesity-induced bone resorption gene expression has yet to be investigated. Thus, we conducted this study in the context of obesity, employing a high-fat diet-induced obese mouse model. Obese mice treated with a selective and non-selective COX-2 inhibitor (celecoxib and aspirin), significantly (p < 0.05) reduced adipogenic markers such as body and fat weight, serum lipids, mRNA expression of pro-inflammatory markers (COX-2, TNF-α, IL-6, and MCP-1) in adipose tissue and bone resorption markers (OPG, RANKL, Cathepsin K, and MMP-9) in tibia bone tissue. In addition, arachidonic acid (AA) supplementation significantly (p < 0.5) increased the expression of obesity-induced inflammatory cytokines in the tibia bone marrow via the COX-2-derived PGE2 signaling pathway, hence increase the osteoclastogenesis. These findings suggested that inhibiting the COX-2 signaling pathway could reduce obesity and inflammatory bone resorption. Although both the selective and non-selective COX inhibitors had similar effects, selective COX-2 was more effective in these events, indicating that COX-2 plays a critical role in obesity-associated inflammatory bone resorption.
肥胖和骨质流失一直是研究的焦点。肥胖刺激脂肪组织扩张和脂肪细胞肥大,导致脂肪细胞慢性低度炎症。增大的脂肪细胞分泌多种促炎化学物质。由于其内分泌信号,这些物质间接促进破骨细胞活动和骨质流失。然而,COX-2信号在肥胖诱导的骨吸收基因表达中的作用尚未被研究。因此,我们在肥胖的背景下进行了这项研究,采用高脂肪饮食诱导的肥胖小鼠模型。用选择性和非选择性COX-2抑制剂(塞来昔布和阿司匹林)治疗的肥胖小鼠,显著(p <; 0.05)降低了脂肪生成标志物,如体重和脂肪重、血清脂质、脂肪组织中促炎标志物(COX-2、TNF-α、IL-6和MCP-1)的mRNA表达以及胫骨骨组织中骨吸收标志物(OPG、RANKL、Cathepsin K和MMP-9)。此外,花生四烯酸(AA)的补充显著(p <; 0.5)通过cox -2来源的PGE2信号通路增加了肥胖诱导的炎症细胞因子在胫骨骨髓中的表达,从而增加了破骨细胞的发生。这些发现表明,抑制COX-2信号通路可以减少肥胖和炎症性骨吸收。尽管选择性和非选择性COX抑制剂具有相似的作用,但选择性COX-2在这些事件中更有效,这表明COX-2在肥胖相关的炎症性骨吸收中起关键作用。
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引用次数: 0
Aspirin-triggered RvD1 (AT-RvD1) modulates epithelial-mesenchymal transition on bronchial epithelial cells stimulated with cigarette smoke extract 阿司匹林触发的RvD1 (AT-RvD1)调节香烟烟雾提取物刺激支气管上皮细胞的上皮-间质转化
IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-02-19 DOI: 10.1016/j.prostaglandins.2025.106968
Aline Beatriz Mahler Pereira , Bethânia Alves Gontijo , Sarah Cristina Sato Vaz Tanaka , Fernanda Bernadelli de Vito , Hélio Moraes de Souza , Paulo Roberto da Silva , Alexandre de Paula Rogerio
The epithelial-mesenchymal transition (EMT) plays significant role in airway remodeling during chronic obstructive pulmonary disease (COPD) and lung cancer. Aspirin-triggered resolvin D1 (AT-RvD1) presents anti-inflammatory and pro-resolution effects, via lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2). In addition, AT-RvD1 prevented TGF-β1-induced EMT in lung cancer cells (A549 cells). Here, we extend these results and evaluated the role of AT-RvD1 in cigarette smoke extract (CSE)-induced EMT on bronchial epithelial cells (BEAS-2B). CSE decreased E-cadherin expression, an epithelial marker, and increased ROS and TGF-β1 productions, and expressions of mesenchymal markers (N-cadherin, vimentin, smad2/3 and slug). Furthermore, CSE induced an increase in the ALX/FPR2 receptor expression. AT-RvD1 restored the expression of E-cadherin and reduced the N-cadherin, Vimentin, smad2/3 and ALX/FPR2 expressions as well as ROS and TGF-β1 productions on CSE-stimulated cells. In conclusion, AT-RvD1 has the potential to control epithelial-mesenchymal transition induced by smoking in the normal lung epithelial cells.
上皮-间质转化(EMT)在慢性阻塞性肺疾病(COPD)和肺癌患者气道重塑中起重要作用。阿司匹林触发的溶解蛋白D1 (AT-RvD1)通过脂素A4受体/甲酰基肽受体2 (ALX/FPR2)具有抗炎和促溶解作用。此外,AT-RvD1可阻止TGF-β1诱导的肺癌细胞(A549细胞)EMT。在这里,我们扩展了这些结果,并评估了AT-RvD1在香烟烟雾提取物(CSE)诱导的支气管上皮细胞(BEAS-2B)的EMT中的作用。CSE降低了上皮标志物E-cadherin的表达,增加了ROS和TGF-β1的产生以及间质标志物(N-cadherin、vimentin、smad2/3和slug)的表达。此外,CSE诱导ALX/FPR2受体表达增加。AT-RvD1恢复了cse刺激细胞E-cadherin的表达,降低了N-cadherin、Vimentin、smad2/3和ALX/FPR2的表达以及ROS和TGF-β1的产生。综上所述,AT-RvD1具有控制吸烟诱导的正常肺上皮细胞上皮-间质转化的潜力。
{"title":"Aspirin-triggered RvD1 (AT-RvD1) modulates epithelial-mesenchymal transition on bronchial epithelial cells stimulated with cigarette smoke extract","authors":"Aline Beatriz Mahler Pereira ,&nbsp;Bethânia Alves Gontijo ,&nbsp;Sarah Cristina Sato Vaz Tanaka ,&nbsp;Fernanda Bernadelli de Vito ,&nbsp;Hélio Moraes de Souza ,&nbsp;Paulo Roberto da Silva ,&nbsp;Alexandre de Paula Rogerio","doi":"10.1016/j.prostaglandins.2025.106968","DOIUrl":"10.1016/j.prostaglandins.2025.106968","url":null,"abstract":"<div><div>The epithelial-mesenchymal transition (EMT) plays significant role in airway remodeling during chronic obstructive pulmonary disease (COPD) and lung cancer. Aspirin-triggered resolvin D1 (AT-RvD1) presents anti-inflammatory and pro-resolution effects, via lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2). In addition, AT-RvD1 prevented TGF-β1-induced EMT in lung cancer cells (A549 cells). Here, we extend these results and evaluated the role of AT-RvD1 in cigarette smoke extract (CSE)-induced EMT on bronchial epithelial cells (BEAS-2B). CSE decreased E-cadherin expression, an epithelial marker, and increased ROS and TGF-β1 productions, and expressions of mesenchymal markers (N-cadherin, vimentin, smad2/3 and slug). Furthermore, CSE induced an increase in the ALX/FPR2 receptor expression. AT-RvD1 restored the expression of E-cadherin and reduced the N-cadherin, Vimentin, smad2/3 and ALX/FPR2 expressions as well as ROS and TGF-β1 productions on CSE-stimulated cells. In conclusion, AT-RvD1 has the potential to control epithelial-mesenchymal transition induced by smoking in the normal lung epithelial cells.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"177 ","pages":"Article 106968"},"PeriodicalIF":2.5,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Changes in the serum phospholipid profile of neuroborreliosis patients, foresters, and patients subjected to long-term therapy according to ILADS methods 根据ILADS方法,神经螺旋体病患者、林业人员和接受长期治疗的患者血清磷脂谱的变化。
IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-02-03 DOI: 10.1016/j.prostaglandins.2025.106966
Wojciech Łuczaj , Anna Moniuszko-Malinowska , Monika Groth , Elżbieta Skrzydlewska
The aim of the study was the assessment of changes in the serum phospholipid profile patients with Lyme neuroborreliosis (NB), asymptomatic people after frequent tick bites and patients after long-term multidrug therapy against B.burgdorferi. LC-QTOF-MS/MS platform was used to identify changes in serum phospholipid profile of 37 persons. The results demonstrate differences PL profile among patients with Lyme borreliosis (LB), people frequently exposed to tick bites and patients treated with long-term multidrug therapy compared to healthy subjects. Significant differences in SM, LPC, PI, and PC content of NB patients discriminate this group of patients from the other groups, have potential diagnostic value, and can be used for the development of more effective diagnostic tools. The finding that the phospholipid profile of foresters is similar to healthy people, suggests the existence of adaptive mechanisms that are currently difficult to explain but are interesting from the perspective of future research.
本研究的目的是评估莱姆病神经螺旋体病(NB)患者、频繁蜱叮咬后无症状人群和长期多药治疗伯氏疏螺旋体患者血清磷脂谱的变化。采用LC-QTOF-MS/MS平台对37人血清磷脂谱的变化进行了分析。结果表明,莱姆病borreliosis (LB)患者、经常接触蜱虫叮咬的人以及长期接受多种药物治疗的患者的PL谱与健康受试者相比存在差异。NB患者的SM、LPC、PI、PC含量存在显著差异,可将本组患者与其他组区分开来,具有潜在的诊断价值,可用于开发更有效的诊断工具。林农的磷脂谱与健康人相似的发现表明,目前难以解释的适应性机制的存在,但从未来研究的角度来看是有趣的。
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引用次数: 0
Epoxyeicosatrienoic acids (EETs): A novel class of second messengers of hormonal functional responses 环氧二碳三烯酸(EETs):一类新的激素功能反应第二信使。
IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-30 DOI: 10.1016/j.prostaglandins.2025.106967
Jorge H. Capdevila , John R. Falck , Adeniyi Michael Adebesin
Epoxyeicosatrienoic acids (EETs) are a class of cytochrome P450 (P450) arachidonic acid (AA) metabolites with diverse biological activities including anti-hypertensive, vasodilatory, angiogenic, and anti-inflammatory properties. While their functions as autocrine and paracrine mediators in cardiovascular and renal systems are well established, their mechanism of action and roles in hormonal functional responses are yet to be fully defined. In this review, we highlight extant evidence of their participation in hormonal transmembrane signal transduction leading to the activation of the ERK1/2 or Akt serine/threonine kinases. Based on studies with EGF (Epidermal Growth Factor), VEGF (Vascular Endothelial Growth Factor) and insulin binding to their membrane bound receptors, we propose to include EETs to the inventory of intracellular mediators associated with the functional responses elicited upon selected hormone/receptor interactions.
环氧二碳三烯酸(EETs)是一类细胞色素P450 (P450)花生四烯酸(AA)代谢物,具有抗高血压、血管扩张、血管生成和抗炎等多种生物活性。虽然它们在心血管和肾脏系统中作为自分泌和旁分泌介质的功能已经确立,但它们在激素功能反应中的作用机制和作用尚未完全确定。在这篇综述中,我们强调了它们参与激素跨膜信号转导导致ERK1/2或Akt丝氨酸/苏氨酸激酶激活的现有证据。基于对表皮生长因子(EGF)、血管内皮生长因子(VEGF)和胰岛素与其膜结合受体结合的研究,我们建议将eet纳入与选定激素/受体相互作用引起的功能反应相关的细胞内介质清单中。
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引用次数: 0
Beta-sitosterol regulates PTGS1 to inhibit gastric cancer cell proliferation and angiogenesis 谷甾醇调节PTGS1抑制胃癌细胞增殖和血管生成。
IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-24 DOI: 10.1016/j.prostaglandins.2025.106964
Jindao Wang , Minghui Zhou , Qiuli Zhou , Guangyang Sun , Yu Zhang , Feng Tao , Minfeng Ye

Background

Gastric cancer (GC) is the third leading culprit of cancer-related deaths around the world. Beta-sitosterol (BS) is an important phytosterol that has been proven to have anti-proliferative effects on GC and other tumors. However, mechanisms and targets of BS in cancer are rarely explored.

Methods

In this investigation, the targets of BS in the treatment of GC were analyzed by network pharmacology. Molecular docking and cellular thermal shift assay were introduced to validate the binding relationship between BS and PTGS1. The impacts of BS on GC cell viability, half maximal inhibitory concentration, proliferation ability, apoptosis level, and angiogenesis ability were detected by using Cell Counting Kit-8, clone formation assay, flow cytometry, and angiogenesis experiment, respectively. In addition, the expression levels of angiogenic factors (VEGF, FGF, PAI-1) were detected by using western blot.

Results

In this project, through cell experiments, PTGS1 was identified as a protein that directly binds to BS. In vitro cell experiments revealed that BS promoted apoptosis and inhibited GC cell proliferation and angiogenesis. Importantly, treatment with BS attenuated the promoting influence of PTGS1 overexpression on GC cell proliferation and angiogenesis.

Conclusion

This investigation highlighted PTGS1 as the target of BS in GC cells. BS can regulate PTGS1 to inhibit GC cell proliferation and angiogenesis, providing new evidence for the potential use of BS as a therapeutic agent for GC.
背景:胃癌(GC)是全球癌症相关死亡的第三大元凶。谷甾醇(BS)是一种重要的植物甾醇,已被证明对胃癌和其他肿瘤具有抗增殖作用。然而,BS在癌症中的作用机制和靶点却很少被探索。方法:采用网络药理学方法对BS治疗GC的作用靶点进行分析。通过分子对接和细胞热移实验验证了BS与PTGS1的结合关系。通过细胞计数试剂盒-8、克隆形成实验、流式细胞术和血管生成实验分别检测BS对胃癌细胞活力、半最大抑制浓度、增殖能力、凋亡水平和血管生成能力的影响。western blot检测血管生成因子(VEGF、FGF、PAI-1)的表达水平。结果:本项目通过细胞实验,鉴定出PTGS1是一种直接结合BS的蛋白。体外细胞实验显示,BS促进胃癌细胞凋亡,抑制胃癌细胞增殖和血管生成。重要的是,BS治疗减弱了PTGS1过表达对GC细胞增殖和血管生成的促进作用。结论:本研究表明PTGS1是GC细胞BS的靶点。BS可调节PTGS1抑制胃癌细胞增殖和血管生成,为BS作为胃癌治疗剂的潜在应用提供了新的证据。
{"title":"Beta-sitosterol regulates PTGS1 to inhibit gastric cancer cell proliferation and angiogenesis","authors":"Jindao Wang ,&nbsp;Minghui Zhou ,&nbsp;Qiuli Zhou ,&nbsp;Guangyang Sun ,&nbsp;Yu Zhang ,&nbsp;Feng Tao ,&nbsp;Minfeng Ye","doi":"10.1016/j.prostaglandins.2025.106964","DOIUrl":"10.1016/j.prostaglandins.2025.106964","url":null,"abstract":"<div><h3>Background</h3><div>Gastric cancer (GC) is the third leading culprit of cancer-related deaths around the world. Beta-sitosterol (BS) is an important phytosterol that has been proven to have anti-proliferative effects on GC and other tumors. However, mechanisms and targets of BS in cancer are rarely explored.</div></div><div><h3>Methods</h3><div>In this investigation, the targets of BS in the treatment of GC were analyzed by network pharmacology. Molecular docking and cellular thermal shift assay were introduced to validate the binding relationship between BS and PTGS1. The impacts of BS on GC cell viability, half maximal inhibitory concentration, proliferation ability, apoptosis level, and angiogenesis ability were detected by using Cell Counting Kit-8, clone formation assay, flow cytometry, and angiogenesis experiment, respectively. In addition, the expression levels of angiogenic factors (VEGF, FGF, PAI-1) were detected by using western blot.</div></div><div><h3>Results</h3><div>In this project, through cell experiments, PTGS1 was identified as a protein that directly binds to BS. <em>In vitro</em> cell experiments revealed that BS promoted apoptosis and inhibited GC cell proliferation and angiogenesis. Importantly, treatment with BS attenuated the promoting influence of PTGS1 overexpression on GC cell proliferation and angiogenesis.</div></div><div><h3>Conclusion</h3><div>This investigation highlighted PTGS1 as the target of BS in GC cells. BS can regulate PTGS1 to inhibit GC cell proliferation and angiogenesis, providing new evidence for the potential use of BS as a therapeutic agent for GC.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"177 ","pages":"Article 106964"},"PeriodicalIF":2.5,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143041091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Lutein, a non-provitamin A carotenoid, reduces cisplatin-induced cardiotoxicity 叶黄素,一种非维生素a原类胡萝卜素,减少顺铂引起的心脏毒性。
IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-22 DOI: 10.1016/j.prostaglandins.2025.106965
Fatih Mehmet Gür , Sedat Bilgiç , İbrahim Aktaş
Cardiovascular complications resulting from cisplatin (CS) are a significant factor that can disrupt the treatment plan associated with this chemotherapy. This information led us to investigate the effectiveness of lutein (LT), which has antioxidant effects, in preventing CS-induced cardiotoxic effects. After 28 rats were randomly divided into four equal groups, saline (1 ml/day) was administered to the control group, LT (100 mg/kg/day) to the LT group, CS (10 mg/kg) to the CS group, and active agents in the LT and CS groups were administered to the CS + LT group in the same dose and manner. The examinations determined that MDA, cardiac biomarkers (CK-MB, BNP, LDH, and cTn-I) levels, TNF-α and caspase-3 expressions, and apoptosis significantly increased in the CS group. In contrast, GSH, SOD, and CAT levels were decreased. In addition, histopathological changes characterized by interstitial edema, leukocyte infiltration, and vacuolar degeneration were detected in the heart tissues of this group. It was determined that LT application prevented the above-mentioned CS-induced cardiotoxic effects to a significant extent, although not completely. The findings obtained in this study show that LT may reduce CS-induced cardiac damage thanks to its ROS-reducing, anti-inflammatory, anti-apoptotic, and cytoprotective characteristics.
顺铂(CS)引起的心血管并发症是一个重要因素,可以破坏与这种化疗相关的治疗计划。这些信息促使我们研究具有抗氧化作用的叶黄素(LT)在预防cs诱导的心脏毒性作用中的有效性。将28只大鼠随机分为4组,对照组给予生理盐水(1ml/d), LT组给予LT (100mg/kg/d), CS组给予CS (10mg/kg), LT组和CS组的活性药物给予CS + LT组相同的剂量和方式。检测发现,CS组MDA、心脏生物标志物(CK-MB、BNP、LDH、cTn-I)水平、TNF-α、caspase-3表达及细胞凋亡均显著升高。相比之下,GSH、SOD和CAT水平降低。此外,心脏组织病理变化表现为间质水肿、白细胞浸润、空泡变性。结果表明,尽管不完全阻止了上述cs诱导的心脏毒性作用,但LT的应用在很大程度上阻止了上述作用。本研究结果表明,LT具有降低ros、抗炎、抗凋亡和细胞保护等特性,可减轻cs诱导的心脏损伤。
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引用次数: 0
The effect of saffron supplementation on liver and kidney function, blood glucose and pressure in patients with diabetes and prediabetes: A grade assessed systematic review and meta-analysis of randomized controlled trials 补充藏红花对糖尿病和前驱糖尿病患者肝肾功能、血糖和血压的影响:随机对照试验的系统评价和荟萃分析。
IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-14 DOI: 10.1016/j.prostaglandins.2025.106949
Jia-Wei Zhang , Qing Zhao , Zhe Li , Qian Liu , Sha-Sha Zang , Sha Liu
Saffron has been traditionally used for various health benefits, but its effects on biomarkers of liver function, kidney function, and blood pressure in diabetes are not well understood. This meta-analysis aims to evaluate the impact of saffron supplementation on systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose (FBG), liver enzymes (ALT, AST), and kidney function markers (BUN, creatinine) in patients with diabetes and prediabetes. A comprehensive search was conducted across multiple databases to identify randomized controlled trials (RCTs) assessing saffron/crocin supplementation on glycemic control, hepatic and renal function, and blood pressure regulation in patients with diabetes and prediabetes. Data were extracted and analyzed using random effects model to determine the effect sizes and 95 % confidence intervals (CIs) for each biomarker. The GRADE framework was employed to assess the certainty of the evidence for each outcome. Thirteen studies were included in the meta-analysis. Saffron supplementation significantly reduced SBP (SMD = −0.57, 95 % CI: −0.8 to −0.34, p = 0.036) with the high certainty of evidence, FBG (SMD = −0.57, 95 % CI: −0.93 to −0.22, p = 0.001) with the low certainty of evidence, and AST (SMD = −0.49, 95 % CI: −0.97 to −0.00, p = 0.049) with the low certainty of evidence. Other studied biomarkers were not affected significantly by saffron/crocin supplementation. Saffron/crocin supplementation is effective in decreasing AST, SBP, and FBG levels in patients with diabetes and prediabetes. However, it has no significant effect on ALT, renal function, and DBP. Our observed effect sizes on AST, SBP, and FBG are not clinically important.
传统上,藏红花被用于各种健康益处,但其对糖尿病患者肝功能、肾功能和血压的生物标志物的影响尚不清楚。本荟萃分析旨在评估补充藏红花对糖尿病和前驱糖尿病患者收缩压(SBP)、舒张压(DBP)、空腹血糖(FBG)、肝酶(ALT、AST)和肾功能指标(BUN、肌酐)的影响。在多个数据库中进行了全面的搜索,以确定评估藏红花/藏红花素补充对糖尿病和糖尿病前期患者血糖控制、肝肾功能和血压调节的随机对照试验(rct)。提取数据并使用随机效应模型进行分析,以确定每种生物标志物的效应大小和95%置信区间(ci)。GRADE框架被用来评估每个结果证据的确定性。13项研究被纳入meta分析。藏红花补充显著降低收缩压(SMD = -0.57, 95% CI: -0.8至-0.34,p = 0.036),证据确定性高,FBG (SMD = -0.57, 95% CI: -0.93至-0.22,p = 0.001),证据确定性低,AST (SMD = -0.49, 95% CI: -0.97至-0.00,p = 0.049)。其他研究的生物标志物没有受到藏红花/藏红花素补充的显著影响。在糖尿病和前驱糖尿病患者中,补充藏红花/藏红花素可有效降低AST、SBP和FBG水平。但对ALT、肾功能、舒张压无明显影响。我们观察到的AST、SBP和FBG的效应大小在临床上并不重要。
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Prostaglandins & other lipid mediators
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